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脂氢过氧化物经光动力作用生成后的膜间转位:氧化还原损伤的传播。

Intermembrane Translocation of Photodynamically Generated Lipid Hydroperoxides: Broadcasting of Redox Damage.

机构信息

Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI.

Department of Biophysics, Jagiellonian University, Krakow, Poland.

出版信息

Photochem Photobiol. 2022 May;98(3):591-597. doi: 10.1111/php.13537. Epub 2021 Nov 9.

DOI:10.1111/php.13537
PMID:34633674
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8995396/
Abstract

Lipid hydroperoxides (LOOHs), including cholesterol- and phospholipid-derived species, are reactive intermediates that arise during photosensitized peroxidation of unsaturated lipids in biological membranes. These intermediates may appear in cancer cell membranes during anti-tumor photodynamic therapy (PDT). Photodynamically generated LOOHs have several different fates, including (a) iron-catalyzed one-electron reduction to free radical species which trigger damaging chain peroxidation reactions, (b) selenoperoxidase-catalyzed two-electron reduction to redox-inert alcohols (LOHs), and (c) spontaneous or protein-mediated translocation to other lipid membrane compartments where (a) or (b) may take place. These different LOOH fates will be described in this review, but with special attention to category (c), which the authors were the first to describe and characterize. Seminal early findings on cholesterol hydroperoxide (ChOOH) translocation and its potential negative consequences will be discussed. In reviewing this work, we wish to congratulate Jean Cadet, for his many outstanding accomplishments as a photobiologist and P&P editor.

摘要

脂氢过氧化物(LOOHs),包括胆固醇和磷脂衍生的物种,是在生物膜中不饱和脂质的光敏过氧化过程中产生的反应性中间产物。这些中间产物可能出现在肿瘤细胞的细胞膜中,在抗肿瘤光动力疗法(PDT)期间。光动力生成的 LOOHs 有几种不同的命运,包括(a)铁催化的单电子还原为自由基物种,引发破坏性的链过氧化反应,(b)硒代过氧化物酶催化的两电子还原为氧化还原惰性醇(LOHs),以及(c)自发或蛋白介导的转运到其他脂质膜隔室,其中(a)或(b)可能发生。本综述将描述这些不同的 LOOH 命运,但特别关注作者首次描述和表征的类别(c)。将讨论胆固醇氢过氧化物(ChOOH)转运及其潜在负面影响的早期重要发现。在回顾这项工作时,我们希望祝贺 Jean Cadet,他作为一名光生物学家和 P&P 编辑取得了许多杰出的成就。

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Nitric Oxide-elicited Resistance to Antitumor Photodynamic Therapy via Inhibition of Membrane Free Radical-mediated Lipid Peroxidation.一氧化氮通过抑制膜自由基介导的脂质过氧化诱导抗肿瘤光动力治疗耐药性。
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